T resident helper cells promote humoral responses in the lung
- Authors
- Swarnalekha, Nivedya; Schreiner, David; Litzler, Ludivine C.; Iftikhar, Saadia; Kirchmeier, Daniel; Kunzli, Marco; Son, Young Min; Sun, Jie; Moreira, Etori Aguiar; King, Carolyn G.
- Issue Date
- Jan-2021
- Publisher
- AMER ASSOC ADVANCEMENT SCIENCE
- Citation
- SCIENCE IMMUNOLOGY, v.6, no.55
- Journal Title
- SCIENCE IMMUNOLOGY
- Volume
- 6
- Number
- 55
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/72082
- DOI
- 10.1126/sciimmunol.abb6808
- ISSN
- 2470-9468
- Abstract
- Influenza is a deadly and costly infectious disease, even during flu seasons when an effective vaccine has been developed. To improve vaccines against respiratory viruses, a better understanding of the immune response at the site of infection is crucial. After influenza infection, clonally expanded T cells take up permanent residence in the lung, poised to rapidly respond to subsequent infection. Here, we characterized the dynamics and transcriptional regulation of lung-resident CD4(+) T cells during influenza infection and identified a long-lived, Bcl6-dependent population that we have termed T resident helper (T-RH) cells. T-RH cells arise in the lung independently of lymph node T follicular helper cells but are dependent on B cells, with which they tightly colocalize in inducible bronchus-associated lymphoid tissue (iBALT). Deletion of Bcl6 in CD4(+) T cells before heterotypic challenge infection resulted in redistribution of CD4(+) T cells outside of iBALT areas and impaired local antibody production. These results highlight iBALT as a homeostatic niche for T-RH cells and advocate for vaccination strategies that induce T-RH cells in the lung.
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Collections - College of Biotechnology & Natural Resource > Department of Systems Biotechnology > 1. Journal Articles
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